Prevention of hospital-acquired hypokalemia in children receiving maintenance fluid therapy

Objective: It has been suggested that the use of hypotonic intravenous fluid (IVF) puts hospitalized children at a greater risk of developing hyponatremia in children with increased arginine vasopressin (AVP) production. To reduce its risk, the National Patient Safety Agency in UK issued alert 22 in 2007, of which recommendations were to use isotonic solutions for these children at risk of hyponatremia, instead of the previously most commonly used IVF (0.18% saline/ 4% dextrose) for maintenance fluid therapy. Recent observations, however, revealed that hypokalemia are also common in hospitalized patients who do not receive potassium in their IVF. This study was conducted to validate the potassium added IVF for the prevention of hospital-acquired hypokalemia in maintenance fluid therapy. Design: For maintenance fluid therapy, a commercially available IVF solution in Japan named as Solita-T2R (Na 84 mmol/L, K 20 mmol/L, Cl 66 mmol/L, glucose 3.2%) was infused for 41 sick children with a median age of 3.01 years. Its composition is close equivalent to 0.45% saline/5% dextrose (Na 77 mmol/L, K 0 mmol/L, Cl 77 mmol/L, dextrose 5%) except K content. The patients in states of AVP excess were excluded from the analysis. Results: Median serum potassium value did not drop significantly at a median interval of 48 hours (before IVF: 4.30 mmol/L, after IVF: 4.10 mmol/L, p > 0.05), whereas median serum sodium level significantly increased from 136.0 mmol/L to 139.0 mmol/L (p < 0.001). Conclusion: Potassium added (20 mmol/L) IVF solution reduces the risk of developing “hospital-acquired hypokalemia” in children who are not in states of AVP excess in maintenance fluid therapy. It is worthwhile to study prospectively in a larger number of sick children.

Pathogenesis of childhood idiopathic nephrotic syndrome:a paradigm shift from T-cells to podocytes

Background:Nephrotic syndrome is the most common cause of kidney disease in children,but its pathogenesis remains unclear.This article reviews the novel aspects of the mechanisms underlying massive proteinuria in minimal-change disease,which is the most common form of childhood nephrotic syndrome.Data sources:This article integrates the findings of a PubMed database search for English language articles published in the past 40 years(from September 1974 to February 2014)using the key words"pathogenesis","minimal change nephrotic syndrome"or"idiopathic ne phrotic syndrome".Results:Unknown humoral factors associated with T-cell dysfunction have been thought to play an important role in the pathogenesis of minimal-change disease.However,recent findings are changing this paradigm,i.e,visceral glomerular epithelial cells(podocytes)may be involved via expression of molecules such as CD80 and angiopoietin-like 4.Conclusions:Recent evidence suggests that minimal-change disease results from interactions between humoral factors and dysfunctional podocytes.In addition to immunosuppressant drugs that target lymphocytes,a biological agent such as an antibody against the abnormal molecule(S)expressed by podocytes may provide novel drug treatment for minimal-change disease.